Arquivos Brasileiros de Endocrinologia & Metabologia
Print version ISSN 0004-2730
NEGRAO, André B. and LICINIO, Julio. Leptina: o diálogo entre adipócitos e neurônios. Arq Bras Endocrinol Metab [online]. 2000, vol.44, n.3, pp. 205-214. ISSN 0004-2730. http://dx.doi.org/10.1590/S0004-27302000000300004.
The discovery of leptin led to a renewed interest in the study of enegy homeostasis. It is now recognized that white adipose tissue is the major site of leptin synthesis. After it is secreted into the bloodstream leptin binds itself to specific receptors in the brain, providing the central nervous system with a satiety signal that reflects the amount of energy stored as fat. Acting through receptors that transduce a signal by the JAK/STAT pathway, leptin modifies the expression and activity of hypothalamic peptides that regulate appetite and energy expenditure. In addition, leptin signals nutritional status to other physiological systems and modulates the function of several target glands. More recently, recombinant leptin was successfully given to an obese patient with leptin deficiency due to a mutation in the ob gene. On the other hand, the effects of recombinant leptin in the only study with obese patients and increased levels of circulating leptin were less impressive. Here we review the complexity of leptin actions with a focus on its integrative role as a signal of nutritional status for the organism.
Keywords : ob Gene; Adipose tissue; Hypothalamus; Energy balance; Obesity.